Arousal deficit shown in aged rat's quantitative EEG and ameliorative action of pramiracetam compared to piracetam

The basal EEG profile of the aged Fisher-344 rat was consistently different from that of the young rat, showing dominant high voltage slow-wave components. These slow waves were present in both the frontal cerebral cortex and dorsal hippocampus. Absent or greatly attenuated in the aged rat's hippocampal EEG was rhythmic theta activity, which was always dominant in the young awake rat's hippocampus. These EEG differences were clearly apparent only under basal test conditions, i.e., following habituation to the test situation. Pramiracetam sulfate acted strongly to normalize the aged rat's EEG, while the action of piracetam was weak and appeared to undergo tolerance development.     

Pharmacologic therapeutic window of pramiracetam demonstrated in behavior,EEG, and single neuron firing rates

Summary Following oral or intravenous administration, a representative cognition activator drug, pramiracetam sulfate, is shown to have a pharmacologic therapeutic window at three different levels of study: learned behavior, gross EEG activity of the frontal cortex and hippocampus, and firing rate of single hippocampal neurons.     

Distribution of monoamine oxidase in hippocampal region of the rat

The distribution and development of type A and type B monoamine oxidase (MAO) activities in the hippocampal region of the rat was investigated with biochemical microdetermination. Type A MAO is absolutely dominant and unevenly distributed in the hippocampus. The development of type A MAO in the hippocampus seems to be delayed and reachs adult levels by the 30th day after birth.     

Distribution of monoamine oxidase in hippocampal region of the rat

Summary The distribution and development of type A and type B monoamine oxidase (MAO) activities in the hippocampal region of the rat was investigated with biochemical microdetermination. Type A MAO is absolutely dominant and unevenly distributed in the hippocampus. The development of type A MAO in the hippocampus seems to be delayed and reachs adult levels by the 30th day after birth.     

Age-dependent change in the ability of protein synthesis,by rat liver microsomes-significance of 2 associated factors

Summary An activator and an inhibitor of polypeptide synthesis were isolated from microsomes of rat liver. The young rat contained a higher level of the activator but a lower level of the inhibitor than the aged rat. The significantly higher ratio of the specific activity of the activator to inhibitor in the young microsomes helps explain the higher capacity for protein synthesis of these microsomes as compared to the microsomes of the aged animal.The author thanks Mrs. M. Guillier for her technical help in this work.     

Action and interaction of two 888-1888-1888-1agonists,methoxamine and St 587, on the rabbit's blood pressure and EEG

Summary In rabbits methoxamine reversed the vasopressor effect of St 587 and abolished the EEG synchronizing action of St 587. The interaction on the blood pressure could be ascribed either to the different chemical structures of St 587 and methoxamine or to partial agonistic properties of St 587. The interaction on the EEG appears to be more complex.     

Modulation of hepatic mitochondrial energy efficiency with age

This study was designed to examine the effect of youth-adulthood transition on hepatic mitochondrial energy efficiency. The changes in basal and palmitate-induced proton leak, which contribute to mitochondrial efficiency, were evaluated in mitochondria isolated from the liver of young and adult rats. Alterations in mitochondrial cytochrome oxidase and aconitase specific activities, and in adenine nucleotide translocator content were also assessed. There was no difference in basal proton leak or thermodynamic coupling and efficiency of oxidative phosphorylation in liver mitochondria between the two rat groups. On the other hand, palmitate-induced proton leak increased significantly in adult rats. The function of this uncoupling could be avoidance of elevated formation of reactive oxygen species, which are known to accelerate ageing.Received 17 February 2004; received after revision 30 March 2004; accepted 1 April 2004     

基于LPC2132和μC／OS-Ⅱ的脑电检测系统设计

本文阐述了脑电检测系统的原理;系统由信号采集单元和以ARM7为核心的中央处理器LPC2132两大部分组成。信号采集单元承担了脑电信号的采集、放大滤波的任务。将处理过的脑电信号送入LPC2132芯片中,对脑电信号进行后续处理。LPC2132所实现的功能有：AD转换、数据存储、显示波形等。由于微处理器所承担的任务多且切换频繁,在内核植入了μC／OS-Ⅱ操作系统。本文详细阐述了在LPC2132微处理器中植入μC／OS-Ⅱ操作系统所要进行必要的设置和任务创建的步骤。     

Pharmacologic therapeutic window of pramiracetam demonstrated in behavior, EEG, and single neuron firing rates

Following oral or intravenous administration, a representative cognition activator drug, pramiracetam sulfate, is shown to have a pharmacologic therapeutic window at three different levels of study: learned behavior, gross EEG activity of the frontal cortex and hippocampus, and firing rate of single hippocampal neurons.     

Peptidergic innervation of the temporomandibular disk in the rat

Summary The peptidergic innervation of the temporomandibular disk was investigated in the postnatal young rat by using an indirect immunofluorescence method. Calcitonin gene-related peptide-containing nerve fibers were located around the blood vessels and terminated as free nerve endings in the disk. These nerve fibers may be of a sensory nature.     

Endocannabinoids and β-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels

We investigated the involvement of endocannabinoids in the control of neuronal damage and memory retention loss in rodents treated with the β-amyloid peptide (1–42) (BAP). Twelve days after stereotaxic injection of BAP into the rat cortex, and concomitant with the appearance in the hippocampus of markers of neuronal damage, 2-arachidonoyl glycerol, but not anandamide, levels were enhanced in the hippocampus. VDM-11 (5 mg/kg, i.p.), an inhibitor of endocannabinoid cellular reuptake, significantly enhanced rat hippocampal and mouse brain endocannabinoid levels when administered sub-chronically starting either 3 or 7 days after BAP injection and until the 12–14th day. VDM-11 concomitantly reversed hippocampal damage in rats, and loss of memory retention in the passive avoidance test in mice, but only when administered from the 3rd day after BAP injection. We suggest that early, as opposed to late, pharmacological enhancement of brain endocannabinoid levels might protect against β-amyloid neurotoxicity and its consequences. Received 26 January 2006; received after revision 24 March 2006; accepted 12 April 2006     

Peptidergic innervation of the temporomandibular disk in the rat

The peptidergic innervation of the temporomandibular disk was investigated in the postnatal young rat by using an indirect immunofluorescence method. Calcitonin gene-related peptide-containing nerve fibers were located around the blood vessels and terminated as free nerve endings in the disk. These nerve fibers may be of a sensory nature.     

Regional cyclic AMP levels in homogenates of rat brain after ketalar and trifluoperazine

There was a significant fall in cAMP levels after administration of TFP or ketalar. Different amounts of cAMP were present in different regions of rat brain. Concentrations of cAMP in different regions of the rat brain were found to decrease in the following order: cerebrum > thalamus with hypothalamus > midbrain > hippocampus > cerebral cortex.     

Action of diphenylhydantoin on chromosomes

The effect of diphenyl hydantoin, (DPH) a nonbarbituate anticonvulsant drug, on chromosomes and fertility was tested in cultured human lymphocytes, mouse fertility, and rat maternal marrow chromosomes and fetal development. Whole human blood from 5 male and 5 female subjects was cultured for 68 hours with phytohemagglutinin, then incubated for 2 hours in isotonic salts with .05-.3 mg per ml DPH, .02 mcg per ml colchicine, or .4 mg per ml sodium diethylbarbiturate. The mean number of metaphases per 1000 stimulated cells was 10.0 in controls, 40.3 with colchicine, 27.9 with diethylbarbiturate, and 30.5 with .25 mg DPH per ml. Both diphenylbarbiturate and DPH produced linear dose effect curves. These results were demonstrated not to be due to urea, since there were no differences in urea content, with a 2 hour urease micromethod. Mouse fertility was totally inhibited in 6 virgin mice given .1mg DPH daily for 10 days compared to 41 pups both of 6 control mice. In 6 pregnant rats given 25 mg DPH per 100 gm/orally 4 times daily for 2 days on gestation Days 7 and 8, there were 5 rats with all fetuses resorbed and 1 rat with 3 living and several resorptions. 6 controls had 6-14 normal fetuses each. 50 metaphase plates from each rat's femoral marrow and each fetus were examined 2 hous after injecting .3 mg colchicine per 100 gm. 30% of the metaphase cells from treated females and fetuses showed strongly contracted chromosomes and reduced number os "pulverized" chromosomes. These phenomena may have been due to inhibition by DPH of folic acid metabolism which is involved in purine synthesis.     

Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus

In the developing brain, nicotinic acetylcholine receptors (nAChRs) are involved in cell survival, targeting, formation of neural and sensory circuits, and development and maturation of other neurotransmitter systems. This regulatory role is disrupted when the developing brain is exposed to nicotine, which occurs with tobacco use during pregnancy. Prenatal nicotine exposure has been shown to be a strong risk factor for memory deficits and other behavioral aberrations in the offspring. The molecular mechanisms underlying these neurobehavioral outcomes are not clearly elucidated. We used a rodent model to assess behavioral, neurophysiological, and neurochemical consequences of prenatal nicotine exposure in rat offspring with specific emphasis on the hippocampal glutamatergic system. Pregnant dams were infused with nicotine (6 mg/kg/day) subcutaneously from the third day of pregnancy until birth. Results indicate that prenatal nicotine exposure leads to increased anxiety and depressive-like effects and impaired spatial memory. Synaptic plasticity in the form of long-term potentiation (LTP), basal synaptic transmission, and AMPA receptor-mediated synaptic currents were reduced. The deficit in synaptic plasticity was paralleled by declines in protein levels of vesicular glutamate transporter 1 (VGLUT1), synaptophysin, AMPA receptor subunit GluR1, phospho(Ser845) GluR1, and postsynaptic density 95 (PSD-95). These results suggest that prenatal nicotine exposure by maternal smoking could result in alterations in the glutamatergic system in the hippocampus contributing to the abnormal neurobehavioral outcomes.     

The effect of physostigmine on (Na++K+)-ATPase activity in different rat brain regions

Summary The activity of (Na⁺+K⁺)-ATPase and acetylcholine esterase were folloed in rat brain cerebral cortex, caudate, thalamus, hippocampus and medulla after i.v. administration of physostigmine. Both enzymes were found to be inhibited in a dose-dependent manner. The most pronounced inhibition of (Na⁺+K⁺)-ATPase was found in caudate. where the highest activity of acetylcholine esterase is found.These studies were supported by a grant from the Union of Science of Republic Serbia, No. 40404-14.     

Regional cyclic AMP levels in homogenates of rat brain after ketalar and trifluoperazine

Summary There was a significant fall in cAMP levels after administration of TFP or ketalar. Different amounts of cAMP were present in different regions of rat brain. Concentrations of cAMP in different regions of the rat brain were found to decrease in the following order: cerebrum > thalamus with hypothalamus > midbrain > hippocampus > cerebral cortex.Conducted under ocntract No 10.4.2 with the Polish Academy of Science.     

Topographical distribution of ATP in rat brain.

Studies on the distribution of ATP in microdissected segments of the rat brain indicate that the nucleotide is concentrated in gray matter, and especially in the thalamus, hippocampus, entorhinal cortex and sensorimotor cortex. These distribution studies in conjunction with previous neuropharmacological studies, support the concept that adenine nucleotides may function as intercellular mediators in various regions of the brain.     

Topographical distribution of ATP in rat brain

Summary Studies on the distribution of ATP in microdissected segments of the rat brain indicate that the nucleotide is concentrated in gray matter, and especially in the thalamus, hypothalamus, hippocampus, entorhinal cortex and sensorimotor cortex. These distribution studies in conjuction with previous neuropharmacological studies, support the concept that adenine nucleotides may function as intercellular mediators in various regions of the brain.     

Long-term sequelae of perinatal asphyxia in the aging rat

Information on the consequences of perinatal asphyxia (PA) on brain morphology and function in the aging rat is missing although several groups have hypothesized that PA may be responsible for neurological and psychiatric deficits in the adult. We therefore decided to study the effects of PA on the central nervous system (CNS) in terms of morphology, immunohistochemistry, neurology and behavior in the aging animal. Hippocampus and cerebellum were evaluated morphologically by histological, immunohistochemical and magnetic resonance imaging and cerebellum also by stereological tests. Neurological function was tested by an observational test battery and rota rod test. Cognitive functions were examined by multiple-T-maze and the Morris water maze (MWM). Increased serotonin transporter (SERT) immunoreactivity in the CA2 region of the hippocampus and a significant difference in the escape latency, when the platform of the MWM was moved to a new location, were observed in asphyxiated rats. We showed that deteriorated cognitive functions accompanied by aberrant expression of hippocampal SERT and impaired relearning are long-term sequelae of perinatal asphyxia, a finding that may form the basis for understanding CNS pathology in the aging subject, animal or human.